Dataset Information

293FT Cell Endogenous FANCA Protein-Protein Interactions

ABSTRACT: Hyperinsulinemia affects 72% of Fanconi anemia (FA) patients and an additional 25% experience lowered glucose tolerance or frank diabetes. The underlying molecular mechanisms contributing to the dysfunction of FA pancreas β cells is unknown. These experiments were performed in 293FT HEK cells as a part of the optimization and validation of the endogenous IP and to establish the FANCA interactome in a non-pancreas cell line to delineate beta cell-specific FANCA interactions.

INSTRUMENT(S): LTQ Orbitrap Velos, Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Early Embryonic Cell

DISEASE(S): Fanconi Anemia Complementation Group A

SUBMITTER: Nicholas Woods

LAB HEAD: Nicholas T. Woods, Ph.D.

PROVIDER: PXD010570 | Pride | 2019-07-25

REPOSITORIES: Pride

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Publications

Delineating the role of FANCA in glucose-stimulated insulin secretion in β cells through its protein interactome.

Lagundžin Dragana D Hu Wen-Feng WF Law Henry C H HCH Krieger Kimiko L KL Qiao Fangfang F Clement Emalie J EJ Drincic Andjela T AT Nedić Olgica O Naldrett Michael J MJ Alvarez Sophie S Woods Nicholas T NT

PloS one 20190828 8

Hyperinsulinemia affects 72% of Fanconi anemia (FA) patients and an additional 25% experience lowered glucose tolerance or frank diabetes. The underlying molecular mechanisms contributing to the dysfunction of FA pancreas β cells is unknown. Therefore, we sought to evaluate the functional role of FANCA, the most commonly mutated gene in FA, in glucose-stimulated insulin secretion (GSIS). This study reveals that FANCA or FANCB knockdown impairs GSIS in human pancreas β cell line EndoC-βH3. To ide ...[more]

PMID: 31461451

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